Activation of sympathoadrenomedullary system increases pulmonary nitric oxide production in the rabbit.

Abstract Nitric oxide (NO) is continuously produced in the lung and can be measured in exhaled gas of different species. To investigate a possible neuro-humoral regulation of pulmonary NO production in vivo we injected veratrine, an activator of Na + channels known to activate the sympathoadrenal system, in anaesthetized, mechanically ventilated and laparotomized rabbits. Exhaled NO concentration increased by 38±3% when plasma adrenaline rose from 12.3±3.1 to 49.5±10.7 pmol ml −1 in response to veratrine (500 μg kg −1 , i.v.). Pretreatment with atenolol, a β 1 -adrenoceptor antagonist (1 mg kg −1 ), or bilateral ligation of adrenal blood vessels inhibited the increase in exhaled NO in response to veratrine. Atenolol also decreased basal NO, suggesting an endogenous regulation of pulmonary NO by adrenaline. Neither phentolamine (1 mg kg −1 ), atropine (1 mg kg −1 ) nor vagotomy inhibited the veratrine-induced pulmonary NO production. These results suggest a role of the sympathoadrenal system in the regulation of pulmonary NO production.